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1.
Chinese Medical Journal ; (24): 3032-3038, 2009.
Article in English | WPRIM | ID: wpr-265964

ABSTRACT

<p><b>BACKGROUND</b>Abnormal apoptosis of pulmonary artery smooth muscle cells (PASMCs) is an important pathophysiological process in the pulmonary artery structural remodeling and pulmonary hypertension. We investigated possible effect of endogenous hydrogen sulfide (H2S) on apoptosis of PASMCs during the development of pulmonary hypertension induced by high pulmonary blood flow.</p><p><b>METHODS</b>Thirty-nine male Sprague-Dawley rats were randomly assigned to 4-week control, 4-week shunt, 4-week shunt + propargylglycine (PPG), 11-week control, 11-week shunt and 11-week shunt + sodium hydrosulfide (NaHS) groups. Rats in 4-week shunt, 4-week shunt + PPG, 11-week shunt and 11-week shunt + NaHS groups underwent an abdominal aorta-inferior vena cava shunt. Rats in 4-week shunt + PPG group were intraperitoneally injected with PPG, an inhibitor of endogenous H2S production, for 4 weeks. Rats in 11-week shunt + NaHS group were intraperitoneally injected with NaHS, a H2S donor, for 11 weeks. Lung tissue H2S was evaluated by sulfide-sensitive electrode. Apoptosis of PASMCs were detected by terminal deoxynucleotidyl transferase mediated dUTP nick end labelling (TUNEL). Expressions of Fas, bcl-2 and caspase-3 in the PASMCs were analyzed with immunochemical staining.</p><p><b>RESULTS</b>Four weeks after the shunting operation, the apoptosis of PASMCs and expression of Fas and caspase-3 were significantly decreased (P < 0.01), but expression of bcl-2 increased significantly (P < 0.01). PPG administration further inhibited the apoptosis of PASMCs, downregulated the expression of Fas and caspase-3 (P < 0.01), but increased the expression of bcl-2 (P < 0.01). After 11 weeks of shunting operation, the apoptosis of PASMCs and expression of Fas and caspase-3 were significantly decreased (P < 0.01), but expression of bcl-2 increased obviously (P < 0.01). NaHS administration significantly increased the apoptosis of PASMCs, upregulated the expression of Fas and caspase-3, but inhibited the expression of bcl-2.</p><p><b>CONCLUSIONS</b>H2S induces the apoptosis of PASMCs in the development of high pulmonary blood flow-induced pulmonary hypertension by activating the Fas pathway and inhibiting the bcl-2 pathway.</p>


Subject(s)
Animals , Male , Rats , Alkynes , Pharmacology , Apoptosis , Blood Flow Velocity , Physiology , Blotting, Western , Glycine , Pharmacology , Hemodynamics , Hydrogen Sulfide , Pharmacology , Hypertension, Pulmonary , Immunohistochemistry , In Situ Nick-End Labeling , Myocytes, Smooth Muscle , Cell Biology , Pulmonary Artery , Cell Biology , Random Allocation , Rats, Sprague-Dawley
2.
Journal of Applied Clinical Pediatrics ; (24)1992.
Article in Chinese | WPRIM | ID: wpr-638693

ABSTRACT

Objective To explore the effect of the ?-blocker —metoprolol on the treatment of vasovagal syncope(VVS) in children.Methods Twenty-nine children with unexplained syncope and positive responses to head-up tilt test(HUT) were included in the study.Sixteen of them took metoprolol(treatment group) and 13 of them took vitamin B or oryzanol (control group) at least 2 weeks and HUT were repeated and syncope episodes were observed.Results In treatment group,9 of 16 patients had no syncope episode while 5 of 16 patients had fewer syncope episodes,1 case had more syncope episodes,and 1 case remained the same.HUT were repeated and 6 of 9 cases had negative outcome.In control group,1 of 13 patients had no syncope episode while 5 of 13 patients had fewer syncope episode,3 cases had more syncope episodes and 4 cases remained the same.HUT were repeated and 3 of 7 cases had ne-(gative) outcome.Conclusion These results indicate that adminstering metoprolol orally may be effective for VVS in children.

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